Objective:To investigate the role of angiotensin Ⅱ(Ang Ⅱ) in the injury of podocytes

last barrier of glomemlar filtration

to research the pathogenesis of diabetic nephropathy.Methods:The experimental rats were divided into three groups:control rats(group C)

diabetic rats(group D)and diabetic rats treated by losartan(group DT).Urinary albumin excretion rate (UAER) was assayed 5 weeks after treatment.In addition

the activity of superoxide dismutase(SOD)

catalase (CAT) and concentration of matondialdehyde(MDA) in renal cortex were measured.The podocyte ultrastructure was observed by transmission electronic microscopy while immunohistochemistry was used to detect the expression of desmin

a marker of podocyte injury.Results:Compared with control rats

the activity of SOD and CAT was decreased significantly and the concentrations of MDA were increased markedly in diabetic renal cortex.The expression of glomerular desmin increased markedly accompanied with foot process effacement in podocytes in diabetic group.At the same time

UAER increased in diabetes.The changes of SOD

CAT

MDA

glomemlar desmin expression

UAER and foot process effacement were markedly ameliorated after diabetic rats were treated by angiotensin Ⅱ type one receptor antagonist losartan.Conclusion:Ang Ⅱ may participate in the structural and functional damage of podocytes

last barrier of glomerular filtration

by increasing renal oxidative stress to injure kidney and accelerate proteinuria in diabetes.